Dr Jenny Brockis » Alzheimer’s

Vaccination against Alzheimer’s? We could be one step closer.

solutions — Sun, 18 Dec 2011 03:13:10 +0000

It’s always good to hear encouraging news, especially when it is about a potential treatment for Alzheimer’s disease. A recent report on the evening news spoke about a vaccine being developed through the University of Sydney.

Associate Professor Lars Ittner from Sydney’s Brain and Mind Research Institute is leading a study into developing a vaccine that targets a specific brain protein called tau that is associated with Alzheimer’s disease and fronto- temporal dementia.

In people with dementia, the tau protein forms what are called neurofibrillary tangles, which leads to neuronal death and loss of brain function.

In this study on mice, the vaccine was shown to slow down the development of further neurofibrillary tangles. There was no effect on those tangles that had already formed. So the prospect is that it might be possible if future development of this vaccine occurs for this to be be used in humans once the diagnosis of dementia has been made, and slow down progression of the disease. It is not a cure, but it could buy the person more time for cognitive functioning and possibly work as a preventative if someone is perceived to be at higher risk of developing dementia.

Other researchers around the world have also been looking to develop a vaccine, one to either target tau or amyloid.

Professor Ittner commented that in many studies, vaccines were being trialled in mice with dementia, prior to the onset of clinical symptoms. This study is the first to show that a vaccine targeting tau can be effective once the disease has set in. It is known that the pathological changes associated with Alzheimer’s disease start many years before the clinical onset of symptoms. Having a treatment to slow down further progression would be huge step in the right direction.

Earlier this year I wrote a blog about a nasal spray being developed to minimise the potential risk of vascular dementia.

Researchers at Georgetown University, Washington D.C have found that if an antibody is given later in the progression of Alzheimer’s the greater the chance that it will trigger brain inflammation.

In their studies, mice with Alzheimer’s symptoms were given an antibody called PFA1, which was designed to clear amyloid from their brains. Those mice with the greatest amount of amyloid present at the beginning of treatment showed a greater inflammatory response. The take home from this was that the greatest benefit to lower the amount of amyloid would be obtained by using it early on i.e. in the early stages of the disease.

In Germany, researchers at the University of Rostock are investigating a protein ABCC1, which has been shown to help remove amyloid from mice brains. They have also been using a drug commonly used for treating nausea and vomiting (thiethylperazine) to activate this protein, suggesting that using this drug could be of potential benefit to prevent the development of amyloid plaques.

In the US, Scott Webster at the Georgia Health Sciences University in Augusta is also working on an Alzheimer’s vaccine. His vaccine is targeted versus two brain proteins: amyloid and RAGE (receptor for advanced glycation end-products). The RAGE protein helps the amyloid get into the brain and contributes to the inflammatory process that the amyloid causes to the brain’s neurons.

Webster’s vaccine is different in that it targets these two proteins. The vaccine uses the body’s own immune system to protect against the overproduction of RAGE and amyloid. His vaccine is different also in that it can be taken orally thus using the gut’s bacteria which are vital to our immune system. Previous vaccines developed elsewhere that have targeted just amyloid, have failed to show benefit in clinical trails and some have also had significant side effects. By targeting the two proteins, Webster is more hopeful that this combination effect will lead to reducing or eliminating the toxic effects of the brain inflammation. Early results in animal studies have been encouraging so far, so the next step will be to use the vaccine trialled in larger animal studies.

With all this amazing work going on around the world we are surely moving closer to having more effective treatments that will be able to stop Alzheimer’s in it’s tracks.

Refs:

Bi M, Ittner A, Ke YD, Götz J, Ittner LM (2011) Tau-Targeted Immunization Impedes Progression of Neurofibrillary Histopathology in Aged P301L Tau Transgenic Mice. PLoS ONE 6(12): e26860. doi:10.1371/journal.pone.0026860

American Friends of Tel Aviv University (2011, February 28). An Alzheimer’s vaccine in a nasal spray?. ScienceDaily. Retrieved December 10, 2011, from http://www.sciencedaily.com¬ /releases/2011/02/110228104310.htm

Markus Krohn, Cathleen Lange, Jacqueline Hofrichter, Katja Scheffler, Jan Stenzel, Johannes Steffen, Toni Schumacher, Thomas Brüning, Anne-Sophie Plath, Franziska Alfen, Anke Schmidt, Felix Winter, Katja Rateitschak, Andreas Wree, Jörg Gsponer, Lary C. Walker, Jens Pahnke. Cerebral amyloid-β proteostasis is regulated by the membrane transport protein ABCC1 in mice. Journal of Clinical Investigation, 2011; DOI: 10.1172/JCI57867

Georgia Health Sciences University (2011, September 26). Research points new way to possible Alzheimer’s vaccine. ScienceDaily. Retrieved December 10, 2011, from http://www.sciencedaily.com¬ /releases/2011/09/110926104609.htm

New Diagnostic Guidelines for Alzheimer’s Disease April 2011

solutions — Mon, 25 Apr 2011 03:29:11 +0000

The study of neuroscience over the last three or more decades has revealed a greater understanding of how our brain works and of what causes dementia including Alzheimer’s disease. Yet the clinical diagnostic guidelines for determining what constitutes Alzheimer’s, have only just been revised after a time span of 27 years.

This update now covers the full spectrum, from the earliest preclinical stages, through mild cognitive impairment, to dementia due to Alzheimer’s pathology.

The guidelines also address for the first time the use of imaging and biochemical markers in blood and spinal fluid to help determine whether changes present are likely to be due to Alzheimer’s. As yet biochemical markers and scans are not being used in the clinical setting, they are still predominantly research tools. However this is likely to be changing in the not too distant future.

One of the key drivers to the updated guidelines has been the need to find good clinical tools to permit early and accurate diagnosis.

Previously Alzheimer’s could only be confirmed following death. Autopsy was used to show the pathological findings of amyloid plaques.
We now know that in Alzheimer’s disease, changes in the brain start developing long before any clinical symptoms are apparent and the symptoms do not always correlate to abnormal findings in the brain.

The National Institute on Aging/Alzheimer’s Association Diagnostic Guidelines for Alzheimer’s disease now covers three distinct stages of Alzheimer’s.

1 The Preclinical Stage.

These guidelines only apply currently to a research setting.
In the preclinical stage, brain changes are starting to develop, including accumulation of amyloid and some other nerve cell changes. Significant clinical symptoms are not apparent at this stage. PET scan and CSF analysis may detect the amyloid build up in some people. It remains unknown what the risk of progression of to Alzheimer’s is from this. There is much research continuing into the potential use of biomarkers in a clinical setting.

2 Mild Cognitive Impairment.

These guidelines are also mostly for research. Here a person is recognised to be suffering from memory problems but not in such a way to be impairing their daily functioning.
Not everyone with MCI will progress to full blown Alzheimer’s disease. The use of biomarkers here, is looking for evidence of increased tau protein or decreased levels of beta amyloid in the CSF, reduced glucose uptake in the brain (shown on PET scan) and atrophy of certain parts of the brain (using MRI scans)

3 Alzheimer’s dementia.

Here the clinical manifestations include (in addition to memory loss,) decline in word finding, visuo-spatial difficulty and impaired reasoning or judgement (higher levels of cognition).
Biomarker tested here can be used to increase or decrease the level of certainty about a diagnosis and to differentiate the dementia of Alzheimer’s from other forms of dementia.

This new framework will allow for new findings to be incorporated as discovered. So fortunately, we are unlikely to have to wait for another 27 years before any further revision occurs.

Ref:
NIH/National Institute on Ageing. April 19, 2011 in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association.

What gets up your nose: a spray to prevent Alzheimer’s?

solutions — Mon, 07 Mar 2011 00:54:55 +0000

Are there some things, which really get up your nose?

Well this may be one thing you do want to put up there: a nasal spray capable of protecting your brain from Alzheimer’s disease or stroke.

And before you dismiss that notion as being ridiculous and from “la-la land”, it appears that researchers from Tel Aviv University may be onto something completely novel; a way of effectively preventing and treating Alzheimer’s disease delivering medication via a nasal spray.

This is a story reminiscent of the story of Viagra. The treatment for erectile dysfunction started life as a medication being developed for men with chest pain.
In this case the nasal spray was being developed as a treatment for influenza. The medical scientists were looking to induce an immune response vs. influenza and what they found was that the vaccine, caused the body to activate part of its defence mechanism against viral and other invaders, called macrophages. These macrophages act as large vacuum cleaners gobbling up unwanted proteins such as amyloid from the brain’s blood vessels. Amyloid can build up in the brain and is a pathological finding commonly found in the brain of people with Alzheimer’s disease. In animal studies, once these amyloid proteins had been cleared, then further damage to the brain could be prevented and existing damage repaired.

This means that it may be possible to repair the damage to a brain from a previous stroke and to be able to effectively treat people already experiencing symptoms associated with Alzheimer’s disease.

Previous studies into Alzheimer’s disease have looked at using an immune mediated approach using anti-inflammatory medications and steroids.

Here the immune response being induced is preventing small bleeds causing stroke, which can cause permanent brain damage and contribute to vascular dementia.

The next stage is to look at clinical trials.

So far the animal studies have shown no toxic side effects and fMRI scans on the mice confirmed the effectiveness of the vaccine in returning those mice with cognitive impairment to normal behaviour.

If the drug is found to produce the same effect in humans, this means there may be a simple way of treating up to 80% of those with Alzheimer’s dementia.

Wow, the findings from this study imply we could be looking at a possible breakthrough for a vaccine to guard against and an effective treatment for Alzheimer’s.
Something simple, hopefully inexpensive and literally brain saving.

One small spray for your brain, one giant water cannon of hope for many minds.

Ref: Dr D. Frankel. Tel Aviv Department of Neurobiology Press release

Should you be using HRT to ward off dementia?

solutions — Thu, 27 Jan 2011 22:02:17 +0000

As a baby boomer with a number of baby boomer friends, there have been a couple of questions which come up regularly when we ladies are discussing menopause.

Does HRT (hormone replacement therapy) help preserve your memory and is it safe to take it for that?

Menopause is that wonderful time in a woman’s life where the monthly reminder of periods gradually fades away. This in itself is not usually an issue for most women.
What can be an issue though, is the huge array of associated, assorted symptoms that can accompany that phase.

One of the symptoms not commonly mentioned in the text-books or Doctor’s office, but one not infrequently discussed in our girls talks, is the issue of memory. In an unkind reminder of “pregnancy brain” what we now have raising it’s ugly head is “menopause brain”.
Yes, we seem to be “losing it”. Forgetting appointments, misplacing everything from the car keys to the occasional child, and stressing that not only are now entering that new phase of maturity called “middle age” we also think we might well be losing our mind at the same time.

By the time we reach our late forties and early fifties, that creeping awareness of one’s own mortality starts to develop. We notice our parents are ageing, sometimes becoming very sick or dying. Some of those parents may develop Alzheimer’s disease or dementia, and the sudden emergence of our own memory’s shortgivings can lead us to worry that we too may be at risk.

Moreover, it is known that people with Alzheimer’s and their caregivers are more likely to be women.
Maria Shriver brought home that message very clearly in her report “Women- the face of Alzheimer’s” last year.

So should we be using HRT to help save our memories?
How long should we take it for?
Does it actually make any difference?

Professor Andrew Kaunitz nicely answered these questions in an article from the Department of Obstetrics and Gynaecology, University of Florida College of Medicine.

He writes about a “critical window” of opportunity to use HRT.

In peri menopause, (the time leading up to periods actually finishing) or early menopause, using HRT is associated with a reduced risk of dementia.

However, women who start using HRT in later life actually gain no benefit and may in fact be doing harm.

A long-term cohort study from California published their findings late last year.
In this study, menopausal women aged between 40 and 55 and free of dementia, were between the years of 1963 and 1974 asked whether of not they used HRT. This was determined as being “mid life use”.

Women were again assessed some twenty five to thirty years after the mid life assessment, to see if they were using HRT. If so, they were counted as “late life” users.

Interestingly, what the group found was that those women who had only used HRT in the “mid life” had the lowest prevalence of dementia.
Those who had only used it in “later life” had the highest prevalence of dementia.

Those who had started in midlife and essentially just carried on had a prevalence similar to those women who had never used HRT at all.

Professor Kaunitz says he now advises his clients in the peri menopausal and early menopause that HRT may lower their future risk of dementia with the aim to gradually taper the dose over time and to either eventually discontinue the treatment entirely or suggest they remain on a very low dose. The total length of use also being determined by a number of other individual factors.

Meanwhile, perhaps we should also being looking to see how much relief HRT gives women afflicted by “menopausal brain”. The answer to that question may help women to then decide whether they want to use HRT either as a potential risk modifying agent of dementia, or purely for symptom relief of the “mid life brain”.

Ref:
Whitmer RA, Quesenberry CP, Zhou J, Yaffe K. Timing of hormone therapy and dementia: The critical window theory revisited. Ann Neuro. 2010 Nov 12

Addicted to fat? It’s damaging your brain

solutions — Thu, 20 Jan 2011 22:51:13 +0000

Are you addicted to fast food?

Do you crave that next slice of pizza or double beef burger with bacon?
Is your mouth watering at the thought of chicken and chips?

We know that eating too much fat, especially the bad fats such as trans fats and excess cholesterol, is bad for our hearts and our health.
Too much fat in the form of cholesterol is also really bad for our brain.

But surely when it comes to food choices it just boils down to personal taste, convenience, and availability doesn’t it?

Maybe not.

It turns out that many of us have a “fatty” or “salt” tooth rather than a “sweet” one.

Eating a high fat diet over a period of time has been shown to induce irreversible changes in rat studies in relation to the “pleasure centres” of the brain.

These are the same reward or pleasure centres as activated by heroin and cocaine.

So yes, it seems that we can indeed become addicted to fatty foods.

Back to those rats and their high fat diet. Over a six month period, the genes associated with reward were found to be altered, leading to the animals then craving those particular types of food when no longer available.

Which means that if you are trying to lose weight, but have previously being eating a diet high in fat, it is going to be much harder to say “no” to that temptation, next time it is wafted in front of your nose.

This could be why some people find it so hard when trying to lose weight to adhere to healthier eating in the longer term.

Our brain makes its own cholesterol that it uses to form synapses and brain cell membranes. But if our diet incorporates a high level of excess fat over a period of time, this leads to brain damage.

Rats fed excess fat in their diets over a 5 month period produced changes in their brains resembling Alzheimer’s pathology, with the formation of amyloid plaques and neurofibrillary tangles. They also showed evidence of memory impairment, loss of neurons, micro bleeds into the brain and inflammation.

Alzheimer’s is a complex neurological condition, and while cholesterol on its own is not responsible for causing it, it is certainly a contributing factor.

A second study gave rats a high fat, low Omega-3 diet. Omega-3s are essential fatty acids that we have to obtain from our food, as our body does not produce them. They are found in fish, meat, eggs and walnuts. Omega 3s are essential for normal brain function as they form part of the cell membrane around each neuron and help to maintain a healthy brain and normal cognition.

This combination diet led to brains developing x8.7 the amount of amyloid and x1.5 the amount of tau protein build up compared to controls.

So if you have that fat addiction, how can you resist that slice of oh-so-gooey and delicious looking chocolate mud cake?
And how about those piping hot chips sprinkled with salt?
Perhaps understanding that it is an addiction will help those affected to try and tackle the issue differently.

Following on from this research my question now is: what effect is this chronic high fat diet having on our kids’ brains?

Are we setting our children up for a lifetime of difficulty in weight control and contributing to their risk of developing cognitive problems or neurodegenerative disease in the future?

What are your thoughts?

Refs:
Society for Neuroscience (2011, January 19). Long-term, high-fat diet alters mice brains: Brain changes may contribute to cycles of weight gain. ScienceDaily. Retrieved January 20, 2011, from http://www.sciencedaily.com¬ /releases/2010/11/101115112727.htm

Université Laval (2008, October 31). High-fat Diet Could Promote Development Of Alzheimer’s Disease. ScienceDaily. Retrieved January 20, 2011, from http://www.sciencedaily.com¬ /releases/2008/10/081028103107.htm

Celine Ullrich, Michael Pirchl, Christian Humpel. Hypercholesterolemia in rats impairs the cholinergic system and leads to memory deficits. Molecular and Cellular Neuroscience, 2010; 45 (4): 408 DOI: 10.1016/j.mcn.2010.08.001

Keep those synapses firing: Could this be the key to understanding the origin of brain diseases?

solutions — Mon, 03 Jan 2011 00:27:52 +0000

One of the key findings in Alzheimer’s disease is a loss of synaptic connections.
The synapse is the place where brain cells communicate with each other via their dendritic branches. The cells do not actually touch but are separated by a space called the synaptic cleft. It is across this space that brain chemicals or neurotransmitters cross to stimulate the adjoining brain cells and trigger further electrical messages to be passed along forming neural circuits or pathways.

Without synapses brain cells are unable to communicate to each other.

Sorry, I’m going to get a bit technical here, but it’s important to help understand the article.
Sets of particular proteins that bind together to form a molecular hub called the postsynaptic density or PSD occur at the synapse, in the terminals of the dendrites. Animal studies had previously shown that the PSD plays an important role in brain disease and behaviour. However until now, little has been known about the human PSD.

Researchers from the Welcome Trust Sanger Institute and Edinburgh University have used a technique called proteomics to extract PSD’s from the synapses of patients undergoing brain surgery. Their findings are quite remarkable.

They have discovered a total of 1461 proteins, each encoded by a different gene in these human synapses.
This then allowed them to systematically identify those diseases that affect the human synapse.

Professor Grant who led the research team revealed that over 130 brain diseases involve the PSD including Alzheimer’s, Parkinson’s, some forms of autism and learning disability.

Professor Noebels, Professor of Neurology, Neuroscience and Human Genetics at Baylor College of medicine said that of the 1461 proteins identified, “every seventh protein is involved in a known clinical disorder and half of them are repeat offenders. Researchers will now have a strategic starting point to start to unravel the complexity of brain disorders”

The research group has also created a first molecular network to show just how many of the proteins and diseases are interconnected.

As a sign of tremendous collaboration and desire to accelerate further discovery and use of this data, the scientists have released all of their findings into a public domain at their website G2Cdb
No wikileaks required here. It’s all there to be shared.

They suggest that the proteome of the PSD will help us to gain further understanding of the brain in the same way that the genome assisted our understanding of DNA.

Other fascinating findings Include:

• That the proteins in PSD are important for certain cognitive behaviours such as learning, memory, emotion and mood

• And also for social behaviours, addiction and drug abuse.

Looking at how the PSD has evolved over time and contrary to expectations, the researchers discovered that the PSD has been resistant to change over the millennia.
This means that synapses of rodents are not that dissimilar from humans, making further research using rat and mice models very suitable for studying human brain disease. Looks like we have more in common with our rodent friends than previously recognised.

These findings provide further valuable clues adding to our understanding of the brain and how some brain diseases may develop.

Àlex Bayés, Louie N van de Lagemaat, Mark O Collins, Mike D R Croning, Ian R Whittle, Jyoti S Choudhary, Seth G N Grant. Characterisation of the proteome, diseases and evolution of the human postsynaptic density. Nature Neuroscience, December 19, 2010 DOI: 10.1038/nn.2719

What’s the story about diabetes, cholesterol and your brain?

solutions — Mon, 06 Dec 2010 02:00:10 +0000

Diabetes is a recognised risk factor for dementia.
It is also associated with a higher risk of depression and eating disorders.
What has now been found is that diabetes affects how much cholesterol our brain can make.

That’s right, our brain makes it’s own cholesterol that it uses to form synapses (the connections between brain cells). It is also used to form the vesicles or storage structures located at the synapse that contain the neurotransmitters, the brain’s chemicals that are passed from one brain cell to the next. We have a “fat” head and it is essential the brain can produce sufficient cholesterol for healthy brain function. Having too little cholesterol in the brain is associated with Alzheimer’s disease and other neurodegenerative conditions.

Studies using mice with type 1 (insulin deficient) diabetes looked at gene expression in an area of the brain called the hypothalamus. It was found that in these mice, gene expression for the synthesis of cholesterol was reduced. Treating them using insulin reversed the problem.
They also found that those mice with unable to synthesise brain cholesterol gained more weight and ate more, indicating that diabetes may affect those brain hormones associated with appetite regulation.

This finding adds to our understanding of the relationship between diabetes, cholesterol and healthy brain function. If you have diabetes, having tight glycaemic (sugar) control and maintaining a healthy weight are essential to help your overall brain health and to protect against future cognitive decline.

Ryo Suzuki, Kevin Lee, Enxuan Jing, Sudha B. Biddinger, Jeffrey G. McDonald, Thomas J. Montine, Suzanne Craft, C. Ronald Kahn. Diabetes and Insulin in Regulation of Brain Cholesterol Metabolism. Cell Metabolism, Volume 12, Issue 6, 567-579, 1 December 2010 DOI: 10.1016/j.cmet.2010.11.006

DHA (fish oil) Of No Benefit Once Alzheimer’s Disease Is Present.

solutions — Fri, 05 Nov 2010 01:11:26 +0000

A study has just been published in JAMA which found that giving supplements of Omega-3 (DHA) to people with mild to moderate Alzheimer’s disease did not produce any reduction in the rate of cognitive decline, indicating that supplementation in this group would not be warranted.
In this study a group of 402 people with either mild to moderate Alzheimer’s disease, 60% of the group received supplementation of 2 gm of DHA, the other 40% received placebo over an 18-month period. They underwent cognitive testing using the Alzheimer’s Disease Assessment Scale and Clinical Dementia Rating. A sub sample of 102 subjects also underwent functional MRI scanning to look for the rate of cortical atrophy.
The study found no benefit of the supplementation on the ADAS-Cog score or rate of brain atrophy during the time of the trial.
Many people currently take Omega-three’s as a supplement, commonly as fish oil capsules and include fish in their diet on the basis of other studies, which have suggested that this is a way to reduce one’s personal risk of developing dementia or Alzheimer’s disease .
So should we stop doing this?

Absolutely not. The difference here in this study is that they were looking at people who had been already diagnosed with Alzheimer’s.

An earlier study in 2006 at the respected Karolinska Institute had previously looked to see if DHA and EPA (Omega-3) supplements given to a group of people with either diagnosed Alzheimer’s disease or a small sub-group with very early cognitive impairment would be useful as a means of slowing the progression of the disease. This study also found no benefit of supplementation in those already diagnosed with Alzheimer’s.
However those who only had mild cognitive impairment did show some benefit. They had less cognitive decline on mental testing than a control group over a 6-month period, and when the control group received the supplements over a second 6-month period their rate of decline decreased as well. Here the authors proposed that is may be because the omega-3 fatty acids exert an anti–inflammatory effect. Inflammation is believed to be part of the neuropathological development of Alzheimer’s. The comment then was perhaps the anti-inflammatory effect of the Omega-3’s could only be of use prior to too much neuropathological change being evident.
The 2006 study only included a very small number of subjects (32 people) Larger studies with bigger cohorts of those with mild cognitive impairment as well as those at risk of Alzheimer’s are needed to see if Omega 3-s may be of benefit in halting the earlier progression of the disease.
The conclusion from the latest study supports the literature that supplementation with DHA is not beneficial in established mild to moderate Alzheimer’s.

Meanwhile there is plenty of evidence to support continuing to enjoy eating fish and taking Omega-3 supplements as a means of reducing our relative risk of developing cognitive decline and dementia.

Bon appetit!

Journal References:
1. K. Yaffe. Treatment of Alzheimer Disease and Prognosis of Dementia: Time to Translate Research to Results. JAMA: The Journal of the American Medical Association, 2010; 304 (17): 1952 DOI: 10.1001/jama.2010.1625
2. J. F. Quinn, R. Raman, R. G. Thomas, K. Yurko-Mauro, E. B. Nelson, C. Van Dyck, J. E. Galvin, J. Emond, C. R. Jack, M. Weiner, L. Shinto, P. S. Aisen. Docosahexaenoic Acid Supplementation and Cognitive Decline in Alzheimer Disease: A Randomized Trial. JAMA: The Journal of the American Medical Association, 2010; 304 (17): 1903 DOI: 10.1001/jama.2010.1510
3. JAMA and Archives Journals (2006, October 11). Omega-3 Fatty Acids May Slow Cognitive Decline In Some Patients With Very Mild Alzheimer’s Disease. ScienceDaily. Retrieved November 4, 2010, from http://www.sciencedaily.com¬ /releases/2006/10/061010022736.htm

Are today’s 70 year olds smarter than their predecessors?

solutions — Thu, 28 Oct 2010 09:16:41 +0000

Are we getting more intelligent?

That’s a question I’m sure we would all like to assume to be answered with a “Yes”. However is there any proof of this?

Well it turns out that in Sweden there has been an ongoing study doing intelligence tests on 70 year olds and the findings do actually show that, yes the 70 year olds of today do perform better in these tests than their predecessors of thirty years ago.

And there are probably a number of contributing factors such as
• Improved pre and neonatal care
• Improved nutrition
• Better quality of education
• Better treatment of hypertension and other vascular diseases
• Higher intellectual requirements of today’s society with access to advanced technology, the Internet and television.

But that wasn’t the main reason for conducting this study.
What the researchers were looking for was to see if they could find a better way to predict who is most likely to develop dementia and whether the early symptoms have changed over recent generations.

One thing that the study did reveal too is that the incidence of dementia has remained unchanged over this period of 30 years.
People aged 70 to 75 today have the same incidence of dementia as those of that age group 30 years ago. This is important because with the expected explosion of people likely to be diagnosed with Alzheimer’s disease over the next forty years, it would be possible to assume that Alzheimer’s is becoming more common. The increase is actually simply a reflection of the larger proportion of people in our society reaching that age.

In this study of over 2000 people the only predictor of dementia was found to be those with memory problems. But not all of those with memory problems went on to develop dementia.

The researchers were looking to identify those at risk of developing dementia and while they found pointers for a group born in 1901-1902 the same tests did not reveal any clues for the generation born in 1930. It is hoped that finding earlier signs of dementia will enable people more at risk to get diagnosed earlier and receive support more quickly.

S. Sacuiu, D. Gustafson, M. Sjogren, X. Guo, S. Ostling, B. Johansson, I. Skoog. Secular changes in cognitive predictors of dementia and mortality in 70-year-olds. Neurology, 2010; 75 (9): 779 DOI: 10.1212/WNL.0b013e3181f0737c

Our brain reveals it has a second way to store memory.

solutions — Fri, 08 Oct 2010 02:26:01 +0000

This week Bryce Vissel from the Sydney Garvan Institute of Medial Research was on ABC radio discussing the results of the study that had been published in the 29th September edition of PLoS One.

Researchers from Australia and the States have identified a new way that the brain can create memories and store information. The implication of this is that this new pathway may prove useful to provide new and alternative ways of treatments where there has been brain injury or death, such as with stroke and Alzheimer’s disease.

The way our brain works to store memories involves the hippocampus where an essential mechanism called the NMDA receptor is involved. When the NMDA receptor is activated, calcium is allowed to enter the brain cell, which then triggers further molecular reactions resulting in our brain being able to process, store and recall information.
Our understanding over the last twenty or thirty years has been that learning could not take place without these receptors. The scientists were looking to replicate the mechanism artificially and coincidentally uncovered an existing second system that the brain already has in place. In this second system a different receptor called AMPA does the job of encoding memory, but appears only to be activated when the information received is similar to something we have previously learnt. This is called second learning.

The questions now being raised from this finding is to work out what causes this second mechanism to operate. Then it may be possible to look for ways to get it to take over the role of the NMDA mechanism if that isn’t working because of disease or injury.
It might then be used to protect us against conditions such as Alzheimer’s (where the ability to form new memories is lost), because it could be that stimulation of this alternative pathway would then help us to keep participating in memories.
The other potential implication of this finding is that having this second means of learning could have really important effects on how we approach teaching in the classroom in the future as well.

Ref: A Role for Calcium Permeable AMPA Receptors in Synaptic Plasticity and Learning.
Wiltgen BJ, Royle GA, Gray EE, Abdipranoto A, Thangthaeng N, et al. 2010 A Role for Calcium-Permeable AMPA Receptors in Synaptic Plasticity and Learning. PLoS ONE 5(9): e12818. doi:10.1371/journal.pone.0012818

Dr Jenny Brockis » Alzheimer’s

Vaccination against Alzheimer’s? We could be one step closer.

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